Acanthoic acid ameliorates lipopolysaccharide-induced acute lung injury

作者：Wang Qiushi; Li Guanghua; Xu Guangquan^*

来源：European Journal of Pharmacology, 2015, 750: 32-38.

DOI：10.1016/j.cfphar.2015.01.023

• Acanthoic acid
• LPS
• Acute lung injury
• NF-kappa B
• LXR alpha

Acanthoic acid, a pimaradiene diterpene isolated from Acanthopanax koreantim, has been reported to have anti-inflammatory activities. However, the effects of acanthoic acid on LPS-induced acute lung injury have not been reported. The purpose of this study was to investigate the protective effect of acanthoic acid on LPS-induced ALI and to clarify the possible anti-inflammatory mechanisms. In vivo, an LPS-induced ALI model in mice was used to assess the protective effects of acanthoic acid on ALL Meanwhile, mouse alveolar macrophages MH-S were stimulated with LPS in the presence or absence of acanthoic acid. The expressions of TNF-alpha, IL-6 and IL-1 beta were measured by ELBA. LXR alpha and NF-kappa B expression were detected by Western blot analysis. The results showed that acanthoic acid down-regulated LPS-induced TNF-alpha, IL-6 and IL-1 beta production in BALE. MPO activity and lung wet-to-dry ratio were also inhibited by acanthoic acid. In addition, acanthoic acid attenuated lung histopathologic changes. In vitro, acanthoic acid inhibited inflammatory cytokines TNF-alpha, IL-6 and IL-1 beta production and NE-kappa B activation in LPS-stimulated alveolar macrophages. Acanthoic acid was found to up-regulated the expression of LXRa. The inhibition of acanthoic acid on LPS-induced cytokines and NF-kappa B activation can be abolished by LXRa siRNA. In conclusion, our results suggested that the protective effect of acanthoic acid on LPS-induced ALI was due to its ability to activate LXRa, thereby inhibiting [PS-induced inflammatory response.

• 出版日期2015-3-5
• 单位哈尔滨医科大学